Sequentially expressed temporal transcription factors in neural stem cells during early development determine which progeny can undergo malignant transformation upon dedifferentiation.

Mitochondrial dysfunction in neural stem cells and brain tumour cells decreases proliferation and affects the generation of neuronal diversity and tumour heterogeneity.

Odd-paired (opa) is required for the progression of temporal patterning in Drosophila neural progenitors to regulate temporal identities via an incoherent feed-forward loop.

Network propagation connects TWIST1 with epigenetic regulators CHD7, CHD8, and WHSC1, which collectively promote the bias toward neural crest while suppressing neural stem cell programmes, and subsequently enhance ectomesenchyme potential.

About twenty temporal patterning genes are identified that drive an irreversible differentiation trajectory governing the heterogeneity and proliferative properties of cells in neural tumors with an early developmental origin.

Semaphorin7A sculpts the collective arbor architecture of the lateral line nerve and facilitates neural contacts with the hair cells for synaptogenesis during neuromast development in the zebrafish.

Genetic analyses combining photoconvertible cell signalling reporters with gain- and loss-of function manipulations reveal a novel role for Notch signalling in controlling Hedgehog response in neural progenitor cells.

Shh, produced by postmitotic spinal neurons, plays crucial roles in the specification of the lateral motor column of the spinal cord through ARHGAP36.

SHH signaling acts through FOXF1/2 transcription factors and antagonizes BMP signaling to specify oral fate and pattern the oral-aboral axis of the mandibular arch to ensure proper formation of jaws.

In addition to a neural crest cell specific role, AP-2α and AP-2ß cooperatively promote craniofacial development through regulating chromatin and gene expression dynamics in the facial surface ectoderm.